肿瘤抑素影响血管瘤内皮细胞凋亡的相关机制分析  

Effect mechanism of tumstatin on the apoptosis process in hemangioma vascular endothelial cell

作　　者：方兴[1] 唐尚鸿[1] 梅文静[1] 曾雪飞[1] 

机构地区：[1]惠州市中心人民医院儿童重症病区,广东惠州516000

出　　处：《临床和实验医学杂志》2018年第4期370-373,共4页Journal of Clinical and Experimental Medicine

摘　　要：目的研究肿瘤抑素对血管瘤内皮细胞的增殖与凋亡过程的调节作用,为临床婴幼儿血管瘤的治疗提供参考。方法血管瘤内皮细胞培养后随机分为5组:对照组、PD98059组、肿瘤抑制素低剂量、中剂量和高剂量组。除对照组给予生理盐水外,其余各组给予PD98059(10μM)处理2 h,肿瘤抑制素低剂量、中剂量和高剂量组分别给予1μM、10μM、100μM的肿瘤抑制素处理2 h。免疫印迹法或荧光定量法分析各组细胞凋亡相关蛋白Caspase3/9、ERK信号通路关键蛋白ERK1/2和MEK及氧化应激蛋白NOX4的表达,DHE染色法分析各组细胞的氧化应激状态。结果与对照组相比,PD98059组血管瘤内皮细胞内ROS水平明显降低、细胞凋亡蛋白Caspase3/9的表达明显升高;同时ERK信号通路关键蛋白的表达明显增强,而肿瘤抑制素低剂量、中剂量和高剂量组作用与PD98059作用一致,且具有剂量依从性。结论肿瘤抑制素通过激活氧化应激状态、ERK信号及抑制细胞凋亡蛋白通过发挥对血管瘤内皮细胞增殖的抑制作用。Objective The present research aimed to explore the effect mechanism of tumstatin on the apoptosis process in hemangioma vascular endothelial cell. Methods Hemangioma vascular endothelial cells were divided into 5 groups： control,PD95059 group and tumstatin group at low,medium and high dose. The cells were treated with PD98059 for 2 h at 10 μM concentration except control. The tumstatin group cells were treated with tumstatin at 1 μM,10 μM,100 μM concentration for 2 h. The expression of NOX4,Caspase3/9,ERK and MEK was detected by Western Blotting or Real-time PCR. The ROS content in each group was assayed by DHE staining. Results The content of ROS was decreased in PD98059 medication group. The expression of Caspase3/9 was increased while the NOX4 expression was decreased in PD98059 medication group. The results also showed that the ERK signaling pathway proteins was increased after medication of in PD98059 medication. These abnormalities were normalized greatly after the medication of tumstatin with a dose dependent manner. Conclusion Oxidative-stress and apoptosis are involved in the tumstatin induced proliferation inhibition of hemangioma vascular endothelial cell.

关 键 词：血管瘤内皮细胞 肿瘤抑素 细胞凋亡 氧化应激 DHE染色 

分 类 号：R732.2[医药卫生—肿瘤]